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• W2124293721 abstract "Patients with congenital adrenal hyperplasia (CAH) receive glucocorticoids as replacement therapy. Glucocorticoid therapy is the most frequent cause of drug-induced osteoporosis.The objective of the study was to evaluate bone mineral density (BMD) and bone metabolism in CAH patients.This was a cross-sectional observational study.The study was conducted at a referral center for pediatric endocrinology.Thirty young patients with the classical form of CAH (aged 16.4-29.7 yr) treated with glucocorticoid from diagnosis (duration of treatment 16.4-29.5 yr) and 138 healthy controls (aged 16.0-30.0 yr) were enrolled.BMD was measured in the lumbar spine and whole body by dual-energy x-ray absorptiometry. Bone formation and resorption rates were estimated by serum measurements of bone-specific alkaline phosphatase and C-terminal telopeptide of type I collagen, respectively.CAH patients were shorter than controls (women -6.8 and men -13.3 cm). Therefore, several methods were used to account for the effect of this difference on bone measurements. Whole-body BMD measurements were significantly lower, compared with controls (P < 0.03), after controlling for height (on average -2.5% in females and -9.3% in male patients). No differences were found in lumbar spine measurements. Bone-specific alkaline phosphatase and C-terminal telopeptide of type I collagen serum concentrations were higher in CAH patients than control subjects (P < 0.04). BMD measurements and bone metabolism markers did not correlate with the actual glucocorticoid dose or mean dose over the previous 7 yr.Young adult patients with the classical form of CAH have decreased bone density values, compared with healthy controls. This may put them at risk of developing osteoporosis early in life." @default.
• W2124293721 created "2016-06-24" @default.
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• W2124293721 date "2006-11-01" @default.
• W2124293721 modified "2023-10-15" @default.
• W2124293721 title "Reduced Bone Mineral Density and Increased Bone Metabolism Rate in Young Adult Patients with 21-Hydroxylase Deficiency" @default.
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• W2124293721 doi "https://doi.org/10.1210/jc.2005-2823" @default.
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